Abstract:Objective - ToinvestigatetheeffectofchrysotileasbestosongeneexpressioninhumanbronchialepithelialBEAS 2B Methods - cells. BEAS 2B cells were randomly divided into two groups. The cells in the chrysotile malignant transformation- groupweretreatedwith 20μg/cm²chrysotiletoestablishthechrysotileinducedmalignanttransformationBEAS 2Bcellmodel, andthecellsinthecontrolgroupweretreatedwiththesamevolumeofphosphatesaltbuffersolution.ThetotalRNAinthecells--wasextractedandthecDNAwassynthesizedbyreversetranscription.Cy5dCTPandCy3dCTPfluoresceinwereusedtolabel the two groups to prepare probes for chip scanning. LuxScan 3.0 image analysis software was used to analyze the fluorescence signal of labeled DNA, and the differentially expressed genes were screened. The Kyoto Encyclopedia of Genes and Genomes Results (KEGG) signaling pathway analysis and Gene Ontology (GO) enrichment analysis were carried out. There were 642 - - differentiallyexpressedgenes(193up regulatedand449down regulated)inchrysotilemalignanttransformationgroupcompared with the control group. The KEGG signaling pathway analysis and GO enrichment analysis showed that the differentially - expressed genes in the malignant transformed BEAS 2B cells induced by chrysotile asbestos were mainly involved in P53 - signaling pathway, histone H3 K9 methylation and methylenetetrahydrofolate reductase deficiency pathway, phosphoinositide binding protein 3 activated protein kinase B signaling pathway, nucleoside phosphate metabolism process and the expression Conclusion inhibitionofhistocompatibilitycomplexⅡantigenpresentation. Chrysotileasbestoscaninducethechangeofgene - - expression profile in BEAS 2B cells. The P53 signaling pathway, histone H3 K9 methylation and other related pathways are